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Cotton, courtesy of the USDA.
What do electrons have to do with our ability to spin this into yarn?
Image via Wikimedia Commons.

by Chris Gunter, Science Education Editor, DXS

Plants are hard. Not in the physical way, but in the genomics way: It’s been estimated that 75% of domesticated plant genomes are polyploid, meaning they have up to 12 sets of each chromosome in every cell. This makes genome sequencing crazily difficult: Each gene segment is represented multiple times, and each one has changes between them, since these organisms multiplied their chromosomes millions of years ago.

Every genome sequence has errors produced along the way; it’s just a factor of the technology and the scale involved. When you are trying to read the genome of a plant and you see a nucleotide position with multiple bases supposedly reported by the sequencer at that position, how do you know what’s real and what’s error?

Enter comparative genomics. Scientists around the world are attacking this problem by sequencing as many different plants as possible and comparing the genomes to each other across evolutionary time. This week, the plant in the spotlight is cotton, or the Gossypium genus. Scientists from 10 countries collaborated to produce a draft genome sequence for Gossypium raimondii, which produces a non-spinnable variety of cotton fiber.

The cotton genome produced is much larger than other plants that have been sequenced – poplar, rice, and grapevines – and in this case 61% of its genome size comes from repetitive elements, which are also quite hard to incorporate into a genome sequence. It’s a little like putting together a multi-million piece jigsaw puzzle where over half the picture is blue sky. In the unique parts of the genome are over 37,000 genes, which is at least 10,000 more than humans.

By comparing this more complete genome sequence to other plants, the researchers can conclude that what we now know as cotton has gone through multiple transformations. At least 60 million years ago, its ancestors diverged from other plants and went through an abrupt chromosome multiplication, to have the five or six sets of chromosomes we still see today.

Then, about 5-10 million years ago, fibers with a structure that allowed them to be spinnable into yarn evolved in some cotton subgroups and not others. To investigate what makes spinnable cotton, the researchers produced some genome sequence for a number of representatives of these subgroups. Intriguingly, they saw linkage between fiber quality and a block of mitochondrial genes that had transported to the nucleus of some cotton strains. Mitochondria are the structures in the cell that take nutrient energy and package it into molecules that cells can use as an energy source.

In the case of cotton, the co-opted mitochondrial genes relate to the way cells like ours and those of plants generate those energy-containing molecules, by transport of electrons through certain enzymes (like NADH dehydrogenase for you aficionados). There is no obvious connection between the observations about electrons and the spinnability of cotton, though, leaving open the question: Can this passage of electrons from protein to protein really be involved in allowing our own ancestors to start making clothes from cotton? Now that these genome data have been released, anyone can study them for an answer.

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The four basic categories of molecules for building life are carbohydrates, lipids, proteins, and nucleic acids.

Carbohydrates serve many purposes, from energy to structure to chemical communication, as monomers or polymers.

Lipids, which are hydrophobic, also have different purposes, including energy storage, structure, and signaling.

Proteins, made of amino acids in up to four structural levels, are involved in just about every process of life.

The nucleic acids DNA and RNA consist of four nucleotide building blocks, and each has different purposes.

The longer version

Life is so diverse and unwieldy, it may surprise you to learn that we can break it down into four basic categories of molecules. Possibly even more implausible is the fact that two of these categories of large molecules themselves break down into a surprisingly small number of building blocks. The proteins that make up all of the living things on this planet and ensure their appropriate structure and smooth function consist of only 20 different kinds of building blocks. Nucleic acids, specifically DNA, are even more basic: only four different kinds of molecules provide the materials to build the countless different genetic codes that translate into all the different walking, swimming, crawling, oozing, and/or photosynthesizing organisms that populate the third rock from the Sun.

Big Molecules with Small Building Blocks

The functional groups, assembled into building blocks on backbones of carbon atoms, can be bonded together to yield large molecules that we classify into four basic categories. These molecules, in many different permutations, are the basis for the diversity that we see among living things. They can consist of thousands of atoms, but only a handful of different kinds of atoms form them. It’s like building apartment buildings using a small selection of different materials: bricks, mortar, iron, glass, and wood. Arranged in different ways, these few materials can yield a huge variety of structures.

We encountered functional groups and the SPHONC in Chapter 3. These components form the four categories of molecules of life. These Big Four biological molecules are carbohydrates, lipids, proteins, and nucleic acids. They can have many roles, from giving an organism structure to being involved in one of the millions of processes of living. Let’s meet each category individually and discover the basic roles of each in the structure and function of life.

Carbohydrates

You have met carbohydrates before, whether you know it or not. We refer to them casually as “sugars,” molecules made of carbon, hydrogen, and oxygen. A sugar molecule has a carbon backbone, usually five or six carbons in the ones we’ll discuss here, but it can be as few as three. Sugar molecules can link together in pairs or in chains or branching “trees,” either for structure or energy storage.

When you look on a nutrition label, you’ll see reference to “sugars.” That term includes carbohydrates that provide energy, which we get from breaking the chemical bonds in a sugar called glucose. The “sugars” on a nutrition label also include those that give structure to a plant, which we call fiber. Both are important nutrients for people.

Sugars serve many purposes. They give crunch to the cell walls of a plant or the exoskeleton of a beetle and chemical energy to the marathon runner. When attached to other molecules, like proteins or fats, they aid in communication between cells. But before we get any further into their uses, let’s talk structure.

The sugars we encounter most in basic biology have their five or six carbons linked together in a ring. There’s no need to dive deep into organic chemistry, but there are a couple of essential things to know to interpret the standard representations of these molecules.

Check out the sugars depicted in the figure. The top-left molecule, glucose, has six carbons, which have been numbered. The sugar to its right is the same glucose, with all but one “C” removed. The other five carbons are still there but are inferred using the conventions of organic chemistry: Anywhere there is a corner, there’s a carbon unless otherwise indicated. It might be a good exercise for you to add in a “C” over each corner so that you gain a good understanding of this convention. You should end up adding in five carbon symbols; the sixth is already given because that is conventionally included when it occurs outside of the ring.

On the left is a glucose with all of its carbons indicated. They’re also numbered, which is important to understand now for information that comes later. On the right is the same molecule, glucose, without the carbons indicated (except for the sixth one). Wherever there is a corner, there is a carbon, unless otherwise indicated (as with the oxygen). On the bottom left is ribose, the sugar found in RNA. The sugar on the bottom right is deoxyribose. Note that at carbon 2 (*), the ribose and deoxyribose differ by a single oxygen.

The lower left sugar in the figure is a ribose. In this depiction, the carbons, except the one outside of the ring, have not been drawn in, and they are not numbered. This is the standard way sugars are presented in texts. Can you tell how many carbons there are in this sugar? Count the corners and don’t forget the one that’s already indicated!

If you said “five,” you are right. Ribose is a pentose (pent = five) and happens to be the sugar present in ribonucleic acid, or RNA. Think to yourself what the sugar might be in deoxyribonucleic acid, or DNA. If you thought, deoxyribose, you’d be right.

The fourth sugar given in the figure is a deoxyribose. In organic chemistry, it’s not enough to know that corners indicate carbons. Each carbon also has a specific number, which becomes important in discussions of nucleic acids. Luckily, we get to keep our carbon counting pretty simple in basic biology. To count carbons, you start with the carbon to the right of the non-carbon corner of the molecule. The deoxyribose or ribose always looks to me like a little cupcake with a cherry on top. The “cherry” is an oxygen. To the right of that oxygen, we start counting carbons, so that corner to the right of the “cherry” is the first carbon. Now, keep counting. Here’s a little test: What is hanging down from carbon 2 of the deoxyribose?

If you said a hydrogen (H), you are right! Now, compare the deoxyribose to the ribose. Do you see the difference in what hangs off of the carbon 2 of each sugar? You’ll see that the carbon 2 of ribose has an –OH, rather than an H. The reason the deoxyribose is called that is because the O on the second carbon of the ribose has been removed, leaving a “deoxyed” ribose. This tiny distinction between the sugars used in DNA and RNA is significant enough in biology that we use it to distinguish the two nucleic acids.

In fact, these subtle differences in sugars mean big differences for many biological molecules. Below, you’ll find a couple of ways that apparently small changes in a sugar molecule can mean big changes in what it does. These little changes make the difference between a delicious sugar cookie and the crunchy exoskeleton of a dung beetle.

Sugar and Fuel

A marathon runner keeps fuel on hand in the form of “carbs,” or sugars. These fuels provide the marathoner’s straining body with the energy it needs to keep the muscles pumping. When we take in sugar like this, it often comes in the form of glucose molecules attached together in a polymer called starch. We are especially equipped to start breaking off individual glucose molecules the minute we start chewing on a starch.

Double X Extra: A monomer is a building block (mono = one) and a polymer is a chain of monomers. With a few dozen monomers or building blocks, we get millions of different polymers. That may sound nutty until you think of the infinity of values that can be built using only the numbers 0 through 9 as building blocks or the intricate programming that is done using only a binary code of zeros and ones in different combinations.

Our bodies then can rapidly take the single molecules, or monomers, into cells and crack open the chemical bonds to transform the energy for use. The bonds of a sugar are packed with chemical energy that we capture to build a different kind of energy-containing molecule that our muscles access easily. Most species rely on this process of capturing energy from sugars and transforming it for specific purposes.

Polysaccharides: Fuel and Form

Plants use the Sun’s energy to make their own glucose, and starch is actually a plant’s way of storing up that sugar. Potatoes, for example, are quite good at packing away tons of glucose molecules and are known to dieticians as a “starchy” vegetable. The glucose molecules in starch are packed fairly closely together. A string of sugar molecules bonded together through dehydration synthesis, as they are in starch, is a polymer called a polysaccharide (poly = many; saccharide = sugar). When the monomers of the polysaccharide are released, as when our bodies break them up, the reaction that releases them is called hydrolysis.

Double X Extra: The specific reaction that hooks one monomer to another in a covalent bond is called dehydration synthesis because in making the bond–synthesizing the larger molecule–a molecule of water is removed (dehydration). The reverse is hydrolysis (hydro = water; lysis = breaking), which breaks the covalent bond by the addition of a molecule of water.

Although plants make their own glucose and animals acquire it by eating the plants, animals can also package away the glucose they eat for later use. Animals, including humans, store glucose in a polysaccharide called glycogen, which is more branched than starch. In us, we build this energy reserve primarily in the liver and access it when our glucose levels drop.

Whether starch or glycogen, the glucose molecules that are stored are bonded together so that all of the molecules are oriented the same way. If you view the sixth carbon of the glucose to be a “carbon flag,” you’ll see in the figure that all of the glucose molecules in starch are oriented with their carbon flags on the upper left.

The orientation of monomers of glucose in polysaccharides can make a big difference in the use of the polymer. The glucoses in the molecule on the top are all oriented “up” and form starch. The glucoses in the molecule on the bottom alternate orientation to form cellulose, which is quite different in its function from starch.

Storing up sugars for fuel and using them as fuel isn’t the end of the uses of sugar. In fact, sugars serve as structural molecules in a huge variety of organisms, including fungi, bacteria, plants, and insects.

The primary structural role of a sugar is as a component of the cell wall, giving the organism support against gravity. In plants, the familiar old glucose molecule serves as one building block of the plant cell wall, but with a catch: The molecules are oriented in an alternating up-down fashion. The resulting structural sugar is called cellulose.

That simple difference in orientation means the difference between a polysaccharide as fuel for us and a polysaccharide as structure. Insects take it step further with the polysaccharide that makes up their exoskeleton, or outer shell. Once again, the building block is glucose, arranged as it is in cellulose, in an alternating conformation. But in insects, each glucose has a little extra added on, a chemical group called an N-acetyl group. This addition of a single functional group alters the use of cellulose and turns it into a structural molecule that gives bugs that special crunchy sound when you accidentally…ahem…step on them.

These variations on the simple theme of a basic carbon-ring-as-building-block occur again and again in biological systems. In addition to serving roles in structure and as fuel, sugars also play a role in function. The attachment of subtly different sugar molecules to a protein or a lipid is one way cells communicate chemically with one another in refined, regulated interactions. It’s as though the cells talk with each other using a specialized, sugar-based vocabulary. Typically, cells display these sugary messages to the outside world, making them available to other cells that can recognize the molecular language.

Lipids: The Fatty Trifecta

Starch makes for good, accessible fuel, something that we immediately attack chemically and break up for quick energy. But fats are energy that we are supposed to bank away for a good long time and break out in times of deprivation. Like sugars, fats serve several purposes, including as a dense source of energy and as a universal structural component of cell membranes everywhere.

Fats: the Good, the Bad, the Neutral

Turn again to a nutrition label, and you’ll see a few references to fats, also known as lipids. (Fats are slightly less confusing that sugars in that they have only two names.) The label may break down fats into categories, including trans fats, saturated fats, unsaturated fats, and cholesterol. You may have learned that trans fats are “bad” and that there is good cholesterol and bad cholesterol, but what does it all mean?

Let’s start with what we mean when we say saturated fat. The question is, saturated with what? There is a specific kind of dietary fat call the triglyceride. As its name implies, it has a structural motif in which something is repeated three times. That something is a chain of carbons and hydrogens, hanging off in triplicate from a head made of glycerol, as the figure shows. Those three carbon-hydrogen chains, or fatty acids, are the “tri” in a triglyceride. Chains like this can be many carbons long.

Double X Extra: We call a fatty acid a fatty acid because it’s got a carboxylic acid attached to a fatty tail. A triglyceride consists of three of these fatty acids attached to a molecule called glycerol. Our dietary fat primarily consists of these triglycerides.

Triglycerides come in several forms. You may recall that carbon can form several different kinds of bonds, including single bonds, as with hydrogen, and double bonds, as with itself. A chain of carbon and hydrogens can have every single available carbon bond taken by a hydrogen in single covalent bond. This scenario of hydrogen saturation yields a saturated fat. The fat is saturated to its fullest with every covalent bond taken by hydrogens single bonded to the carbons.

Saturated fats have predictable characteristics. They lie flat easily and stick to each other, meaning that at room temperature, they form a dense solid. You will realize this if you find a little bit of fat on you to pinch. Does it feel pretty solid? That’s because animal fat is saturated fat. The fat on a steak is also solid at room temperature, and in fact, it takes a pretty high heat to loosen it up enough to become liquid. Animals are not the only organisms that produce saturated fat–avocados and coconuts also are known for their saturated fat content.

The top graphic above depicts a triglyceride with the glycerol, acid, and three hydrocarbon tails. The tails of this saturated fat, with every possible hydrogen space occupied, lie comparatively flat on one another, and this kind of fat is solid at room temperature. The fat on the bottom, however, is unsaturated, with bends or kinks wherever two carbons have double bonded, booting a couple of hydrogens and making this fat unsaturated, or lacking some hydrogens. Because of the space between the bumps, this fat is probably not solid at room temperature, but liquid.

You can probably now guess what an unsaturated fat is–one that has one or more hydrogens missing. Instead of single bonding with hydrogens at every available space, two or more carbons in an unsaturated fat chain will form a double bond with carbon, leaving no space for a hydrogen. Because some carbons in the chain share two pairs of electrons, they physically draw closer to one another than they do in a single bond. This tighter bonding result in a “kink” in the fatty acid chain.

In a fat with these kinks, the three fatty acids don’t lie as densely packed with each other as they do in a saturated fat. The kinks leave spaces between them. Thus, unsaturated fats are less dense than saturated fats and often will be liquid at room temperature. A good example of a liquid unsaturated fat at room temperature is canola oil.

A few decades ago, food scientists discovered that unsaturated fats could be resaturated or hydrogenated to behave more like saturated fats and have a longer shelf life. The process of hydrogenation–adding in hydrogens–yields trans fat. This kind of processed fat is now frowned upon and is being removed from many foods because of its associations with adverse health effects. If you check a food label and it lists among the ingredients “partially hydrogenated” oils, that can mean that the food contains trans fat.

Double X Extra: A triglyceride can have up to three different fatty acids attached to it. Canola oil, for example, consists primarily of oleic acid, linoleic acid, and linolenic acid, all of which are unsaturated fatty acids with 18 carbons in their chains.

Why do we take in fat anyway? Fat is a necessary nutrient for everything from our nervous systems to our circulatory health. It also, under appropriate conditions, is an excellent way to store up densely packaged energy for the times when stores are running low. We really can’t live very well without it.

Phospholipids: An Abundant Fat

You may have heard that oil and water don’t mix, and indeed, it is something you can observe for yourself. Drop a pat of butter–pure saturated fat–into a bowl of water and watch it just sit there. Even if you try mixing it with a spoon, it will just sit there. Now, drop a spoon of salt into the water and stir it a bit. The salt seems to vanish. You’ve just illustrated the difference between a water-fearing (hydrophobic) and a water-loving (hydrophilic) substance.

Generally speaking, compounds that have an unequal sharing of electrons (like ions or anything with a covalent bond between oxygen and hydrogen or nitrogen and hydrogen) will be hydrophilic. The reason is that a charge or an unequal electron sharing gives the molecule polarity that allows it to interact with water through hydrogen bonds. A fat, however, consists largely of hydrogen and carbon in those long chains. Carbon and hydrogen have roughly equivalent electronegativities, and their electron-sharing relationship is relatively nonpolar. Fat, lacking in polarity, doesn’t interact with water. As the butter demonstrated, it just sits there.

There is one exception to that little maxim about fat and water, and that exception is the phospholipid. This lipid has a special structure that makes it just right for the job it does: forming the membranes of cells. A phospholipid consists of a polar phosphate head–P and O don’t share equally–and a couple of nonpolar hydrocarbon tails, as the figure shows. If you look at the figure, you’ll see that one of the two tails has a little kick in it, thanks to a double bond between the two carbons there.

Phospholipids form a double layer and are the major structural components of cell membranes. Their bend, or kick, in one of the hydrocarbon tails helps ensure fluidity of the cell membrane. The molecules are bipolar, with hydrophilic heads for interacting with the internal and external watery environments of the cell and hydrophobic tails that help cell membranes behave as general security guards.

The kick and the bipolar (hydrophobic and hydrophilic) nature of the phospholipid make it the perfect molecule for building a cell membrane. A cell needs a watery outside to survive. It also needs a watery inside to survive. Thus, it must face the inside and outside worlds with something that interacts well with water. But it also must protect itself against unwanted intruders, providing a barrier that keeps unwanted things out and keeps necessary molecules in.

Phospholipids achieve it all. They assemble into a double layer around a cell but orient to allow interaction with the watery external and internal environments. On the layer facing the inside of the cell, the phospholipids orient their polar, hydrophilic heads to the watery inner environment and their tails away from it. On the layer to the outside of the cell, they do the same.

As the figure shows, the result is a double layer of phospholipids with each layer facing a polar, hydrophilic head to the watery environments. The tails of each layer face one another. They form a hydrophobic, fatty moat around a cell that serves as a general gatekeeper, much in the way that your skin does for you. Charged particles cannot simply slip across this fatty moat because they can’t interact with it. And to keep the fat fluid, one tail of each phospholipid has that little kick, giving the cell membrane a fluid, liquidy flow and keeping it from being solid and unforgiving at temperatures in which cells thrive.

Steroids: Here to Pump You Up?

Our final molecule in the lipid fatty trifecta is cholesterol. As you may have heard, there are a few different kinds of cholesterol, some of which we consider to be “good” and some of which is “bad.” The good cholesterol, high-density lipoprotein, or HDL, in part helps us out because it removes the bad cholesterol, low-density lipoprotein or LDL, from our blood. The presence of LDL is associated with inflammation of the lining of the blood vessels, which can lead to a variety of health problems.

But cholesterol has some other reasons for existing. One of its roles is in the maintenance of cell membrane fluidity. Cholesterol is inserted throughout the lipid bilayer and serves as a block to the fatty tails that might otherwise stick together and become a bit too solid.

Cholesterol’s other starring role as a lipid is as the starting molecule for a class of hormones we called steroids or steroid hormones. With a few snips here and additions there, cholesterol can be changed into the steroid hormones progesterone, testosterone, or estrogen. These molecules look quite similar, but they play very different roles in organisms. Testosterone, for example, generally masculinizes vertebrates (animals with backbones), while progesterone and estrogen play a role in regulating the ovulatory cycle.

Double X Extra: A hormone is a blood-borne signaling molecule. It can be lipid based, like testosterone, or short protein, like insulin.

Proteins

As you progress through learning biology, one thing will become more and more clear: Most cells function primarily as protein factories. It may surprise you to learn that proteins, which we often talk about in terms of food intake, are the fundamental molecule of many of life’s processes. Enzymes, for example, form a single broad category of proteins, but there are millions of them, each one governing a small step in the molecular pathways that are required for living.

Levels of Structure

Amino acids are the building blocks of proteins. A few amino acids strung together is called a peptide, while many many peptides linked together form a polypeptide. When many amino acids strung together interact with each other to form a properly folded molecule, we call that molecule a protein.

For a string of amino acids to ultimately fold up into an active protein, they must first be assembled in the correct order. The code for their assembly lies in the DNA, but once that code has been read and the amino acid chain built, we call that simple, unfolded chain the primary structure of the protein.

This chain can consist of hundreds of amino acids that interact all along the sequence. Some amino acids are hydrophobic and some are hydrophilic. In this context, like interacts best with like, so the hydrophobic amino acids will interact with one another, and the hydrophilic amino acids will interact together. As these contacts occur along the string of molecules, different conformations will arise in different parts of the chain. We call these different conformations along the amino acid chain the protein’s secondary structure.

Once those interactions have occurred, the protein can fold into its final, or tertiary structure and be ready to serve as an active participant in cellular processes. To achieve the tertiary structure, the amino acid chain’s secondary interactions must usually be ongoing, and the pH, temperature, and salt balance must be just right to facilitate the folding. This tertiary folding takes place through interactions of the secondary structures along the different parts of the amino acid chain.

The final product is a properly folded protein. If we could see it with the naked eye, it might look a lot like a wadded up string of pearls, but that “wadded up” look is misleading. Protein folding is a carefully regulated process that is determined at its core by the amino acids in the chain: their hydrophobicity and hydrophilicity and how they interact together.

In many instances, however, a complete protein consists of more than one amino acid chain, and the complete protein has two or more interacting strings of amino acids. A good example is hemoglobin in red blood cells. Its job is to grab oxygen and deliver it to the body’s tissues. A complete hemoglobin protein consists of four separate amino acid chains all properly folded into their tertiary structures and interacting as a single unit. In cases like this involving two or more interacting amino acid chains, we say that the final protein has a quaternary structure. Some proteins can consist of as many as a dozen interacting chains, behaving as a single protein unit.

A Plethora of Purposes

What does a protein do? Let us count the ways. Really, that’s almost impossible because proteins do just about everything. Some of them tag things. Some of them destroy things. Some of them protect. Some mark cells as “self.” Some serve as structural materials, while others are highways or motors. They aid in communication, they operate as signaling molecules, they transfer molecules and cut them up, they interact with each other in complex, interrelated pathways to build things up and break things down. They regulate genes and package DNA, and they regulate and package each other.

As described above, proteins are the final folded arrangement of a string of amino acids. One way we obtain these building blocks for the millions of proteins our bodies make is through our diet. You may hear about foods that are high in protein or people eating high-protein diets to build muscle. When we take in those proteins, we can break them apart and use the amino acids that make them up to build proteins of our own.

Nucleic Acids

How does a cell know which proteins to make? It has a code for building them, one that is especially guarded in a cellular vault in our cells called the nucleus. This code is deoxyribonucleic acid, or DNA. The cell makes a copy of this code and send it out to specialized structures that read it and build proteins based on what they read. As with any code, a typo–a mutation–can result in a message that doesn’t make as much sense. When the code gets changed, sometimes, the protein that the cell builds using that code will be changed, too.

Biohazard!The names associated with nucleic acids can be confusing because they all start with nucle-. It may seem obvious or easy now, but a brain freeze on a test could mix you up. You need to fix in your mind that the shorter term (10 letters, four syllables), nucleotide, refers to the smaller molecule, the three-part building block. The longer term (12 characters, including the space, and five syllables), nucleic acid, which is inherent in the names DNA and RNA, designates the big, long molecule.

DNA vs. RNA: A Matter of Structure

DNA and its nucleic acid cousin, ribonucleic acid, or RNA, are both made of the same kinds of building blocks. These building blocks are called nucleotides. Each nucleotide consists of three parts: a sugar (ribose for RNA and deoxyribose for DNA), a phosphate, and a nitrogenous base. In DNA, every nucleotide has identical sugars and phosphates, and in RNA, the sugar and phosphate are also the same for every nucleotide.

So what’s different? The nitrogenous bases. DNA has a set of four to use as its coding alphabet. These are the purines, adenine and guanine, and the pyrimidines, thymine and cytosine. The nucleotides are abbreviated by their initial letters as A, G, T, and C. From variations in the arrangement and number of these four molecules, all of the diversity of life arises. Just four different types of the nucleotide building blocks, and we have you, bacteria, wombats, and blue whales.

RNA is also basic at its core, consisting of only four different nucleotides. In fact, it uses three of the same nitrogenous bases as DNA–A, G, and C–but it substitutes a base called uracil (U) where DNA uses thymine. Uracil is a pyrimidine.

DNA vs. RNA: Function Wars

An interesting thing about the nitrogenous bases of the nucleotides is that they pair with each other, using hydrogen bonds, in a predictable way. An adenine will almost always bond with a thymine in DNA or a uracil in RNA, and cytosine and guanine will almost always bond with each other. This pairing capacity allows the cell to use a sequence of DNA and build either a new DNA sequence, using the old one as a template, or build an RNA sequence to make a copy of the DNA.

These two different uses of A-T/U and C-G base pairing serve two different purposes. DNA is copied into DNA usually when a cell is preparing to divide and needs two complete sets of DNA for the new cells. DNA is copied into RNA when the cell needs to send the code out of the vault so proteins can be built. The DNA stays safely where it belongs.

RNA is really a nucleic acid jack-of-all-trades. It not only serves as the copy of the DNA but also is the main component of the two types of cellular workers that read that copy and build proteins from it. At one point in this process, the three types of RNA come together in protein assembly to make sure the job is done right.

First of all, in the context of science, you should never speak of evolution as a “theory.” There is no theory about whether or not evolution happens. It is a fact.

Scientists have, however, developed tested theories about how evolution happens. Although several proposed and tested processes or mechanisms exist, the most prominent and most studied, talked about, and debated, is Charles Darwin’s idea that the choices of nature guide these changes. The fame and importance of his idea, natural selection, has eclipsed the very real existence of other ways that populations can change over time.

Evolution in the biological sense does not occur in individuals, and the kind of evolution we’re talking about here isn’t about life’s origins. Evolution must happen at least at the populationlevel. In other words, it takes place in a group of existing organisms, members of the same species, often in a defined geographical area.

We never speak of individuals evolving in the biological sense. The population, a group of individuals of the same species, is the smallest unit of life that evolves.

To get to the bottom of what happens when a population changes over time, we must examine what’s happening to the gene combinations of the individuals in that population. The most precise way to talk about evolution in the biological sense is to define it as “a change in the allele frequency of a population over time.” A gene, which contains the code for a protein, can occur in different forms, or alleles. These different versions can mean that the trait associated with that protein can differ among individuals. Thanks to mutations, a gene for a trait can exist in a population in these different forms. It’s like having slightly different recipes for making the same cake, each producing a different version of the cake, except in this case, the “cake” is a protein.

Charles Darwin, who didn’t know anything about alleles or even genes (so now you know more than he did on that score), understood from his work and observations that nature makes certain choices, and that often, what nature chooses in specific individuals turns up again in the individuals’ offspring. He realized that these characteristics that nature was choosing must pass to some offspring. This notion of heredity–that a feature encoded in the genes can be transmitted to your children–is inherent now in the theory of natural selection and a natural one for most people to accept. In science, an observable or measurable feature or characteristic is called a phenotype, and the genes that are the code for it are called its genotype. The color of my eyes (brown) is a phenotype, and the alleles of the eye color genes I have are the genotype.

What is nature selecting any individual in a population to do? In the theory of natural selection, nature chooses individuals that fit best into the current environment to pass along their “good-fit” genes, either through reproduction or indirectly through supporting the reproducer. Nature chooses organisms to survive and pass along those good-fit genes, so they have greater fitness.

Fitness is an evolutionary concept related to an organism’s reproductive success, either directly (as a parent) or indirectly (say, as an aunt or cousin). It is measured technically based on the proportion of an individual’s alleles that are represented in the next generation. When we talk about “fitness” and “the fittest,” remember that fittest does not mean strong. It relates more to a literal fit, like a square peg in a square hole, or a red dot against a red background. It doesn’t matter if the peg or dot is strong, just whether or not it fits its environment.

One final consideration before we move onto a synthesis of these ideas about differences, heredity, and reproduction: What would happen if the population were uniformly the same genetically for a trait? Well, when the environment changed, nature would have no choice to make. Without a choice, natural selection cannot happen–there is nothing to select. And the choice has to exist already; it does not typically happen in response to a need that the environment dictates. Usually, the ultimate origin for genetic variation–which underlies this choice–is mutation, or a change in a DNA coding sequence, the instructions for building a protein.

Don’t make the mistake of saying that an organism adapts by mutating in response to the environment. The mutations (the variation) must already be present for nature to make a choice based on the existing environment.

The Modern Synthesis

When Darwin presented his ideas about nature’s choices in an environmental context, he did so in a book with a very long title that begins, On the Origin of Species by Means of Natural Selection.Darwinknew his audience and laid out his argument clearly and well, with one stumbling block: How did all that heredity stuff actually work?

We now know–thanks to a meticulous scientist named Gregor Mendel (who also was a monk), our understanding of reproductive cell division, and modern genetics–exactly how it all works. Our traits–whether winners or losers in the fitness Olympics–have genes that determine them. These genes exist in us in pairs, and these pairs separate during division of our reproductive cells so that our offspring receive one member or the other of the pair. When this gene meets its coding partner from the other parent’s cell at fertilization, a new gene pair arises. This pairing may produce a similar outcome to one of the parents or be a novel combination that yields some new version of a trait. But this separating and pairing is how nature keeps things mixed up, setting up choices for selection.

With a growing understanding in the twentieth century of genetics and its role in evolution by means of natural selection, a great evolutionary biologist named Ernst Mayr (1904–2005) guided a meshing of genetics and evolution (along with other brilliant scientists including Theodosius Dobzhansky, George Simpson, and R.A. Fisher) into what is called The Modern Synthesis. This work encapsulates (dare I say, “synthesizes?”) concisely and beautifully the tenets of natural selection in the context of basic genetic inheritance. As part of his work, Mayr distilled Darwin’s ideas into a series of facts and inferences.

Facts and Inferences

Mayr’s distillation consists of five facts and three inferences, or conclusions, to draw from those facts.

The first fact is that populations have the potential to increase exponentially. A quick look at any graph of human population growth illustrates that we, as a species, appear to be recognizing that potential. For a less successful example, consider the sea turtle. You may have seen the videos of the little turtle hatchlings valiantly flippering their way across the sand to the sea, cheered on by the conservation-minded humans who tended their nests. What the cameras usually don’t show is that the vast majority of these turtle offspring will not live to reproduce. The potential for exponential growth is there, based on number of offspring produced, but…it doesn’t happen.

The second fact is that not all offspring reproduce, and many populations are stable in size. See “sea turtles,” above.

The third fact is that resources are limited. And that leads us to our first conclusion, or inference: there is a struggle among organisms for nutrition, water, habitat, mates, parental attention…the various necessities of survival, depending on the species. The large number of offspring, most of which ultimately don’t survive to reproduce, must compete, or struggle, for the limited resources.

Fact four is that individuals differ from one another. Look around. Even bacteria of the same strain have their differences, with some more able than others to with stand an antibiotic onslaught. Look at a crowd of people. They’re all different in hundreds of ways.

Fact five is that much about us that is different lies in our genes–it is inheritable. Heredity undeniably exists and underlies a lot of our variation.

So we have five facts. Now for the three inferences:

First, there is that struggle for survival, thanks to so many offspring and limited resources. See “sea turtle,” again.

Second, different traits will be passed on differentially. Put another way: Winner traits are more likely to be passed on.

And that takes us to our final conclusion: if enough of these “winner” traits are passed to enough individuals in a population, they will accumulate in that population and change its makeup. In other words, the population will change over time. It will be adapted to its environment. It will evolve.

When Darwin presented his idea of natural selection, he knew he had an audience to win over. He pointed out that people select features of organisms all the time and breed them to have those features. Darwin himself was fond of breeding pigeons with a great deal of pigeony variety. He noted that unless the pigeons already possessed traits for us to choose, we not would have that choice to make. But we do have choices. We make super-woolly sheep, dachshunds, and heirloom tomatoes simply by selecting from the variation nature provides and breeding those organisms to make more with those traits. We change the population over time.

Darwin called this process of human-directed evolution artificial selection. It made great sense for Darwinbecause it helped his reader get on board. If people could make these kinds of choices and wreak these kinds of changes, why not nature? In the process, Darwin also described this second way evolution can happen: human-directed evolution. We’re awash in it today, from our accidental development of antibiotic-resistant bacteria to wheat that resists devastating rust.

Genetic drift: fixed or lost

What about traits that have no effect either way, that are just there? One possible example in us might be attached earlobes. Good? Bad? Ugly? Well…they don’t appear to have much to do with whether or not we reproduce. They’re just there.

When a trait leaves nature so apparently disinterested, the alleles underlying it don’t experience selection. Instead, they drift in one direction or another, to extinction or 100 percent frequency. When an allele drifts to disappearance, we say that it is lost from the population. When it drifts to 100 percent presence, we say that it has become fixed. This process of evolution by genetic drift reduces variation in a population. Eventually, everyone will have it, or no one will.

Gene flow: genes in, genes out

Another way for a population to change over time is for it to experience a new infusion of genes or to lose a lot of them. This process of gene flow into or out of the population occurs because of migration in or out. Either of these events can change the allele frequency in a population, and that means that gene flow is another was that evolution can happen.

If gene flow happens between two different species, as can occur more with plants, then not only has the population changed significantly, but the new hybrid that results could be a whole new species. How do you think we get those tangelos?

Horizontal gene transfer

One interesting mechanism of evolution is horizontal gene transfer. When we think of passing along genes, we usually envision a vertical transfer through generations, from parent to offspring. But what if you could just walk up to a person and hand over some of your genes to them, genes that they incorporate into their own genome in each of their cells?

Of course, we don’t really do that–at least, not much, not yet–but microbes do this kind of thing all the time. Viruses that hijack a cell’s genome to reproduce can accidentally leave behind a bit of gene and voila! It’s a gene change. Bacteria can reach out to other living bacteria and transfer genetic material to them, possibly altering the traits of the population.

Evolutionary events

Sometimes, events happen at a large scale that have huge and rapid effects on the overall makeup of a population. These big changes mark some of the turning points in the evolutionary history of many species.

The word bottleneck pretty much says it all. Something happens over time to reduce the population so much that only a relatively few individuals survive. A bottleneck of this sort reduces the variability of a population. These events can be natural–such as those resulting from natural disasters–or they can be human induced, such as species bottlenecks we’ve induced through overhunting or habitat reduction.

Founder effect: starting small

Sometimes, the genes flow out of a population. This flow occurs when individuals leave and migrate elsewhere. They take their genes with them (obviously), and the populations they found will initially carry only those genes. Whatever they had with them genetically when they founded the population can affect that population. If there’s a gene that gives everyone a deadly reaction to barbiturates, that population will have a higher-than-usual frequency of people with that response, thanks to this founder effect.

Gene flow leads to two key points to make about evolution: First, a population carries only the genes it inherits and generally acquires new versions through mutation or gene flow. Second, that gene for lethal susceptibility to a drug would be meaningless in a natural selection context as long as the environment didn’t include exposure to that drug. The take-home message is this: What’s OK for one environment may or may not be fit for another environment. The nature of Nature is change, and Nature offers no guarantees.

Hardy-Weinberg: when evolution is absent

With all of these possible mechanisms for evolution under their belts, scientists needed a way to measure whether or not the frequency of specific alleles was changing over time in a given population or staying in equilibrium. Not an easy job. They found–“they” being G. H. Hardy and Wilhelm Weinberg–that the best way to measure this was to predict what the outcome would be if there were no change in allele frequencies. In other words, to predict that from generation to generation, allele frequencies would simply stay in equilibrium. If measurements over time yielded changing frequencies, then the implication would be that evolution has happened.

Defining “Not Evolving”

So what does it mean to not evolve? There are some basic scenarios that must exist for a population not to be experiencing a change in allele frequency, i.e., no evolution. If there is a change, then one of the items in the list below must be false:

·Very large population (genetic drift can be a strong evolutionary mechanism in small populations)

·No migrations (in other words, no gene flow)

·No net mutations (no new variation introduced)

·Random mating (directed mating is one way nature selects organisms)

·No natural selection

In other words, a population that is not evolving is experiencing a complete absence of evolutionary processes. If any one of these is absent from a given population, then evolution is occurring and allele frequencies from generation to generation won’t be in equilibrium.

Convergent Evolution

Arguably the most famous of theegg-laying monotremes, the improbable-seeming platypus. License.

One of the best examples of the influences of environmental pressures is what happens in similar environments a world apart. Before the modern-day groupings of mammals arose, the continent of Australiaseparated from the rest of the world’s land masses, taking the proto-mammals that lived there with it. Over the ensuing millennia, these proto-mammals in Australiaevolved into the native species we see today on that continent, all marsupialsor monotremes.

Among mammals, there’s a division among those that lay eggs (monotremes), those that do most gestating in a pouch rather than a uterus (marsupials), and eutherians, which use a uterus for gestation (placental mammals).

Elsewhere in the world, most mammals developed from a common eutherian ancestor and, where marsupials still persisted, probably outcompeted them. In spite of this lengthy separation and different ancestry, however, for many of the examples of placental mammals, Australiahas a similar marsupial match. There’s the marsupial rodent that is like the rat. The marsupial wolf that is like the placental wolf. There’s even a marsupial anteater to match the placental one.

How did that happen an ocean apart with no gene flow? The answer is natural selection. The environment that made an organism with anteater characteristics best fit in South America was similar to the environment that made those characteristics a good fit in Australia. Ditto the rats, ditto the wolf.

When similar environments result in unrelated organisms having similar characteristics, we call that process convergent evolution. It’s natural selection in relatively unrelated species in parallel. In both regions, nature uses the same set of environmental features to mold organisms into the best fit.

Note: This explanation of evolution and how it happens is not intended to be comprehensive or detailed or to include all possible mechanisms of evolution. It is simply an overview. In addition, it does not address epigenetics, which will be the subject of a different explainer.

Today’s guest post (originally posted here) is from Katie Hinde, an Assistant Professor in Human Evolutionary Biology at Harvard University. Katie studies how variation in mother’s milk influences infant development in rhesus monkeys. You can learn more about Katie and mammalian lactation by visiting her blog, Mammals Suck… Milk!. Follow Katie on Twitter @Mammals_Suck.

Dinosaur Aunts, Bacterial Stowaways, & Insect Milk

Milk is everywhere. From the dairy aisle at the grocery store to the explosive cover of the Mother’s Day issue of Time magazine, the ubiquity of milk makes it easy to take for granted. But surprisingly, milk synthesis is evolutionarily older than mammals. Milk is even older than dinosaurs. Moreover, milk contains constituents that infants don’t digest, namely oligosaccharides, which are the preferred diet of the neonate’s intestinal bacteria (nom nom nom!) And milk doesn’t just feed the infant, and the infant’s microbiome; the symbiotic bacteria are IN mother’s milk.

Evolutionary Origins of Lactation

The fossil record, unfortunately, leaves little direct evidence of the soft-tissue structures that first secreted milk. Despite this, paleontologists can scrutinize morphological features of fossils, such as the presence or absence of milk teeth (diphyodonty), to infer clues about the emergence of “milk.” Genome-wide surveys of the expression and function of mammary genes across divergent taxa, and experimental evo-devo manipulations of particular genes also yield critical insights. As scientists begin to integrate information from complementary approaches, a clearer understanding of the evolution of lactation emerges.

In his recent paper, leading lactation theorist Dr. Olav Oftedal discusses the ancient origins of milk secretion (2012). He contends the first milk secretions originated ~310 million years ago (MYA) in synapsids, a lineage ancestral to mammals and contemporaries with sauropsids, the ancestors of reptiles, birds, and dinosaurs. Synapsids and sauropsids produced eggs with multiple membrane layers, known as amniote eggs. Such eggs could be laid on land. However, synapsid eggs had permeable, parchment-like shells and were vulnerable to water loss. Burying these eggs in damp soil or sand near water resources- like sea turtles do- wasn’t an option, posits Oftedal. The buried temperatures would have likely been too cold for the higher metabolism of synapsids. But incubating eggs in a nest would have evaporated water from the egg. The synapsid egg was proverbially between a rock and a hard place: too warm to bury, too permeable to incubate.

Ophiacodon by Dmitri Bogdanov

Luckily for us, a mutation gave rise to secretions from glandular skin on the belly of the synapsid parent. This mechanism replenished water lost during incubation, allowing synapsids to lay eggs in a variety of terrestrial environments. As other mutations randomly arose and were favored by selection, milk composition became increasingly complex, incorporating nutritive, protective, and hormonal factors (Oftedal 2012). Some of these milk constituents are shunted into milk from maternal blood, some- although also present in the maternal blood stream- are regulated locally in the mammary gland, and some very special constituents are unique to milk. Lactose and oligosaccharides (a sugar with lactose at the reducing end) are two constituents unique to mammalian milk, but are interestingly divergent among mammals living today.

Illustration by Carl Buell

Mammalian and Primate Divergences: Milk Composition

Among all mammals studied to date, lactose and oligosaccharides are the primary sugars in milk. Lactose is synthesized in mammary glands only. Urashima and colleagues explain that lactose synthesis is contingent on the mammalian-specific protein alpha-lactalbumin (2012). Alpha-lactalbumin is very similar in amino-acid structure to C-type lysozyme, a more ancient protein found throughout vertebrates and insects. C-type lysozyme acts as an anti-bacterial agent. Oligosaccharides are predominant in the milks of marsupials and egg-laying monotremes (i.e. the platypus), but lactose is the most prevalent sugar in the milk of most placental (aka eutherian) mammals. Interestingly, the oligosaccharides in the milk of placental mammals are most similar to the oligosaccharides in the milk of monotremes. Unique oligosaccharides in marsupial milk emerged after the divergence of placental mammals.

Marsupial and monotreme young seemingly digest oligosaccharides. Among placental mammals, however, young do not have the requisite enzymes in their stomach and small intestine to utilize oligosaccharides themselves. Why do eutherian mothers synthesize oligosaccharides in milk, if infants don’t digest them?

In May, Anna Petherick’s post “Multi-tasking Milk Oligosaccharides” revealed that oligosaccharides serve a number of critical roles for supporting the healthy colonization and maintenance of the infant’s intestinal microbiome. Beneficial bacterial symbionts contribute to the digestion of nutrients from our food. Just as importantly, they are an essential component of the immune system, defending their host against many ingested pathogens. The structures of milk oligosaccharides have been described for a number of primates, including humans, and data are now available from all major primate clades; strepsirrhines (i.e. lemurs), New World monkey (i.e. capuchin), Old World monkey (i.e. rhesus), and apes (i.e. chimpanzee).

In human milk, there is a much greater diversity and higher abundance of milk oligosaccharides than found in the milk of other primates. Most primate taxa have between 5-30 milk oligosaccharides; humans have ~200. Even more astonishingly, humans predominantly produce Type I oligosaccharides, the preferred food of the most prevalent bacterium in the healthy human infant gut- Bifidobacteria (Urashima et al 2012, Taufik et al. 2012).

Human infants have bigger brains and an earlier age at weaning than do our closest ape relatives. Many anthropologists have hypothesized that constituents in mother’s milk, such as higher fat concentrations or unique fatty acids, underlie these differences in human development. But only oligosaccharides, a constituent that the human infant does not itself utilize, are demonstrably derived from our primate relatives (Hinde and Milligan 2011). At some point in human evolution there must have been strong selective pressure to optimize the symbiotic relationship between the infant microbiome and the milk mothers synthesize to support it. The human and Bifidobacteria genomes show signatures of co-evolution, but the selective pressures and their timing remain to be understood.

Vertical Transmission of Bacteria via Milk

In the womb, the infant is largely protected from maternal bacteria due to the placental barrier. But upon birth, the infant is confronted by a teeming microbial milieu that is both a challenge and an opportunity. The first inoculation of commensal bacteria occurs during delivery as the infant passes through the birth canal and is exposed to a broad array of maternal microbes. Infants born via C-section are instead, and unfortunately, colonized by the microbes “running around” the hospital. But exposure to the mother’s microbiome continues long after birth. Evidence for vertical transmission of maternal bacteria via milk has been shown in rodents, monkeys(Jin et al. 2011), humans(Martin et al. 2012), and… insects.

Yes, INSECTS!

A number of insects have evolved the ability to rely on nutritionally incomplete food sources. They are able to do so because bacteria that live inside their cells provide what the food does not. These bacteria are known as endosymbionts and the specialized cells the host provides for them to live in are called bacteriocytes. For example, the tsetse fly has a bacterium, Wigglesworthia glossinidia,* that provides B vitamins not available from blood meals. Um, if you are squeamish, don’t read the previous sentence.

*I submit the tsetse fly and its bacterial symbiont (Wigglesworthia glossinidia) for consideration as the number one mutualism in which the common name of the host and the Latin name of the bacteria are awesome to say out loud! Bring on your challenger teams.

Hosokawa and colleagues recently revealed the Russian nesting dolls that are bats (Miniopterus fuliginosus), bat flies (Nycteribiidae), and endosymbiotic bacteria (proposed name Aschnera chenzii)(2012). Bat flies are the obligate ectoparasites of bats (Peterson et al. 2007). They feed on the blood of their bat hosts, and for nearly their entire lifespan, bat flies live in the fur of their bat hosts. Females briefly leave their host to deposit pupae on stationary surfaces within the bat roost.

Bat flies are even more crazy amazing because they have a uterus and provide MILK internally through the uterus to larva! Male and female bat flies have endosymbiotic bacteria living in bacteriocytes along the sides of their abdominal segments (revealed by 16S rRNA). Additionally, females host bacteria inside the milk gland tubules, “indicating the presence of endosymbiont cells in milk gland secretion”.

The authors are not yet certain of the specific nutritional role that these bacterial endosymbionts play in the bat fly host. The bacteria may provide B vitamins, as other bacterial symbionts of blood-consuming insects are known to do. My main question is what is the exact role of the bacteria in the milk gland tubules? Are they there to add nutritional value to the milk for the larva, to stowaway in milk for vertical transmission to larva, or both?

Conclusions

The studies described above represent new frontiers in lactation research. The capacity to secrete “milk” has been evolving since before the age of dinosaurs, but we still know relatively little about the diversity of milks produced by mammals today. Even less understood are the consequences and functions of various milk constituents in the developing neonate. Despite the many unknowns, it is increasingly evident that mother’s milk cultivates the infant’s gut bacterial communities in fascinating ways. A microbiome milk-ultivation, if you will, that has far reaching implications for human development, nutrition, and health. Integrating an evolutionary perspective into these newly discovered complexities of milk dynamics allows us to reimagine the world of “dairy” science.